PhotoResearchers from around the world have been working tirelessly towards understanding, and hopefully one day curing, Alzheimer’s disease. While experts still do not understand every facet of the cognitive ailment, a team from Lund University in Sweden may have taken a crucial step towards that goal.

The researchers have found that amyloid plaque, the build-up of which is a marker for Alzheimer’s, is much more versatile than previously suspected. Before now, many believed that the build-up of amyloid plaque was hereditary; in short, if you possessed the gene that caused your body to overproduce amyloid plaque, then you were more likely to develop Alzheimer’s.

However, researchers have found that having this hereditary trait is not necessary for developing the disease. In fact, one does not need any such gene in order to develop Alzheimer’s.

“In our study, we show that accumulation of amyloid in the brain is associated with high levels of specific amyloid peptides in the cerebrospinal fluid,” said Niklas Mattsson, a researcher at Lund University. “This means that overproduction of amyloid beta may contribute to development of Alzheimer’s disease in some people, even if they do not carry the hereditary risk gene for Alzheimer’s.”

Increasing understanding

The researchers made their discovery after examining patients without the hereditary gene for amyloid plaque build-up. Over 330 people participated in the study – they included people with mild cognitive disorders (which can be an indicator for Alzheimer’s) and a control group who had no impairment.

Cerebrospinal fluid samples were collected from each participant and then examined. Results showed that there were increased levels of amyloid beta in some patients in the experimental group, even though they did not have the hereditary gene.

“We were surprised by the results. Our study emphasizes that Alzheimer’s is probably a more heterogeneous disease than we previously believed,” said Mattsson. “The results are important because they increase the understanding of how Alzheimer’s disease arises,” added Oskar Hansson, a reader at Lund University and consultant at Skåne University Hospital.

Possible medical benefits

While future studies will be necessary in order to verify the results, the researchers are hopeful that their work will help in the development of new medications.

“Our hope is that this and other similar studies can increase the possibilities of personalizing treatments that slow down the disease in the future,” said Hansson.

The results of the study have been published in the journal Nature Communications


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